Plants have the ability to recognize the essential chitin molecule present in the fungal cell wall, which stimulates the immune response. Phytopathogenic fungi have developed various strategies to inhibit the chitin-triggered immune response. Here, we identified a chitin deacetylase of Puccinia striiformis f. sp. tritici (Pst), known as PsCDA2, that was induced during the initial invasion of wheat and acted as an inhibitor of plant cell death. Knockdown of PsCDA2 in wheat enhanced its resistance against Pst, highlighting the significance of PsCDA2 in the host-pathogen interaction. Moreover, PsCDA2 can protect Pst urediniospores from being damaged by host chitinase in vitro. PsCDA2 also suppressed the basal chitin-induced plant immune response, including the accumulation of callose and the expression of defence genes. Overall, our results demonstrate that Pst secretes PsCDA2 as a chitin deacetylase involved in establishing infection and modifying the acetyl group to prevent the breakdown of chitin in the cell wall by host endogenous chitinases. Our research unveils a mechanism by which the fungus suppresses plant immunity, further contributing to the understanding of wheat stripe rust control. This information could have significant implications for the development of suitable strategies for protecting crops against the devastating effects of this disease.

As a destructive plant pathogen, Phytophthora infestans secretes diverse host-entering RxLR effectors to facilitate infection. One critical RxLR effector, PiAvr3b, not only induces effector-triggered immunity (ETI), which is associated with the potato resistance protein StR3b, but also suppresses pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI). To date, the molecular basis underlying such dual activities remains unknown. Based on phylogenetic analysis of global P. infestans isolates, we found two PiAvr3b isoforms that differ by three amino acids. Despite this sequence variation, the two isoforms retain the same properties in activating the StR3b-mediated hypersensitive response (HR) and inhibiting necrosis induced by three PAMPs (PiNpp, PiINF1, and PsXeg1) and an RxLR effector (Pi10232). Using a combined mutagenesis approach, we found that the dual activities of PiAvr3b were tightly linked and determined by 88 amino acids at the C-terminus. We further determined that either the W60 or the E134 residue of PiAvr3b was essential for triggering StR3b-associated HR and inhibiting PiNpp- and Pi10232-associated necrosis, while the S99 residue partially contributed to PTI suppression. Additionally, nuclear localization of PiAvr3b was required to stimulate HR and suppress PTI, but not to inhibit Pi10232-associated cell death. Our study revealed that PiAvr3b suppresses the plant immune response at different subcellular locations and provides an example in which a single amino acid of an RxLR effector links ETI induction and cell death suppression.

Efficient plant immune responses depend on the ability to recognise an invading microbe. The 22-amino acids in the N-terminal domain and the 28-amino acids in the central region of the bacterial flagellin, called flg22 and flgII-28, respectively, are important elicitors of plant immunity. Plant immunity is activated after flg22 or flgII-28 recognition by the plant transmembrane receptors FLS2 or FLS3, respectively. There is strong selective pressure on many plant pathogenic and endophytic bacteria to overcome flagellin-triggered immunity. Here we provide an overview of recent developments in our understanding of the evasion and suppression of flagellin pattern recognition by plant-associated bacteria.

Plants adjust amplitude and duration of immune responses via different strategies to maintain growth, development, and resistance to pathogens. Pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI) and effector-triggered immunity (ETI) play vital roles. Pattern recognition receptors, comprising a large number of receptor-like protein kinases and receptor-like proteins, recognize related ligands and trigger immunity. PTI is the first layer of the innate immune system, and it recognizes PAMPs at the plasma membrane to prevent infection. However, pathogens exploit effector proteins to bypass or directly inhibit the PTI immune pathway. Consistently, plants have evolved intracellular nucleotide-binding domain and leucine-rich repeat-containing proteins to detect pathogenic effectors and trigger a hypersensitive response to activate ETI. PTI and ETI work together to protect plants from infection by viruses and other pathogens. Diverse receptors and the corresponding ligands, especially several pairs of well-studied receptors and ligands in PTI immunity, are reviewed to illustrate the dynamic process of PTI response here.[Formula: see text] Copyright © 2021 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license.

The chloroplast has recently emerged as pivotal to co-ordinating plant defence responses and as a target of plant pathogens. Beyond its central position in oxygenic photosynthesis and primary metabolism - key targets in the complex virulence strategies of diverse pathogens - the chloroplast integrates, decodes and responds to environmental signals. The capacity of chloroplasts to synthesize phytohormones and a diverse range of secondary metabolites, combined with retrograde and reactive oxygen signalling, provides exquisite flexibility to both perceive and respond to biotic stresses. These processes also represent a plethora of opportunities for pathogens to evolve strategies to directly or indirectly target \'chloroplast immunity\'. This review covers the contribution of the chloroplast to pathogen associated molecular pattern and effector triggered immunity as well as systemic acquired immunity. We address phytohormone modulation of immunity and surmise how chloroplast-derived reactive oxygen species underpin chloroplast immunity through indirect evidence inferred from genetic modification of core chloroplast components and direct pathogen targeting of the chloroplast. We assess the impact of transcriptional reprogramming of nuclear-encoded chloroplast genes during disease and defence and look at future research challenges.

The cell wall of filamentous fungi, comprised of chitin, polysaccharide and glycoproteins, maintains the integrity of hyphae and protect them from defence responses by potential host plants. Here, we report that one polysaccharide deacetylase of Puccinia striiformis f. sp. tritici (Pst), Pst_13661, suppresses Bax-induced cell death in plants and Pst_13661 is highly induced during early stages of the interaction between wheat and Pst. Importantly, the transgenic wheat expressing the RNA interference (RNAi) construct of Pst_13661 exhibits high resistance to major Pst epidemic races CYR31, CYR32 and CYR33 by inhibiting growth and development of Pst, indicating that Pst_13661 is an available pathogenicity factor and is a potential target for generating broad-spectrum resistance breeding material of wheat. It forms a homo-polymer and has high affinity for chitin and germ tubes of Pst compared with the control. Besides, Pst_13661 suppresses chitin-induced plant defence in plants. Hence, we infer that Pst_13661 may modify the fungal cell wall to prevent recognition by apoplastic surveillance systems in plants. This study opens new approaches for developing durable disease-resistant germplasm by disturbing the growth and development of fungi and develops novel strategies to control crop diseases.

As an obligate parasite, Puccinia striiformis f. sp. tritici (Pst) forms haustoria to obtain nutrients from plant cells for development, and these structures are essential for pathogen survival. To better understand the contribution of haustoria to the interactions with the host plants, we isolated haustoria from susceptible wheat leaves infected with Pst race CYR31 and sequenced their transcriptome as well as those of urediospores and germ tubes, and compared the three transcriptomes. A total of 3524 up-regulated genes were obtained from haustoria, of which 73 genes were related to thiamine biosynthesis, glycolysis and lipid metabolic processes. Silencing seven of the genes reduced the growth and development of Pst in wheat. More interestingly, 1197 haustorial secreted proteins (HASPs) were detected in haustoria, accounting for 34% of the total proteins, indicating that these HASPs play important roles in haustorium-mediated pathogenic progression. Furthermore, 69 HASPs were able to suppress Bax-triggered programmed cell death in tobacco. Additionally, 46 HASPs significantly reduced callose deposition in wheat using the type III secretion system. This study identified a large number of effectors through transcriptome sequencing, and the results revealed components of metabolic pathways that impact the growth and colonization of the pathogen and indicate essential functions of haustoria in the growth and pathogenicity of Pst.

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In the field, plants constantly face a plethora of abiotic and biotic stresses that can impart detrimental effects on plants. In response to multiple stresses, plants can rapidly reprogram their transcriptome through a tightly regulated and highly dynamic regulatory network where WRKY transcription factors can act as activators or repressors. WRKY transcription factors have diverse biological functions in plants, but most notably are key players in plant responses to biotic and abiotic stresses. In tomato there are 83 WRKY genes identified. Here we review recent progress on functions of these tomato WRKY genes and their homologs in other plant species, such as Arabidopsis and rice, with a special focus on their involvement in responses to abiotic and biotic stresses. In particular, we highlight WRKY genes that play a role in plant responses to a combination of abiotic and biotic stresses.

Plants lack the adaptive immune system possessed by mammals. Instead they rely on innate immunity to defend against pathogen attacks. Genomes of higher plants encode a large number of plant immune receptors belonging to different protein families, which are involved in the detection of pathogens and activation of downstream defense pathways. Plant immunity is tightly controlled to avoid activation of defense responses in the absence of pathogens, as failure to do so can lead to autoimmunity that compromises plant growth and development. Many autoimmune mutants have been reported, most of which are associated with dwarfism and often spontaneous cell death. In this review, we summarize previously reported Arabidopsis autoimmune mutants, categorizing them based on their functional groups. We also discuss how their obvious morphological phenotypes make them ideal tools for epistatic analysis and suppressor screens, and summarize genetic screens that have been carried out in various autoimmune mutant backgrounds.